Articles on Medical Diseases and Conditions

Category: Serum Electrolytes and Protein-Calorie Malnutrition

Serum Electrolytes and Protein-Calorie Malnutrition

  • Inappropriate ADH Syndrome (IADH Syndrome)

    This is another syndrome involving AVP (ADH) that is now well recognized. It results from water retention due to secretion of AVP (ADH) when AVP (ADH) would not ordinarily be secreted. The criteria for IADH syndrome include (1) hyponatremia, (2) continued renal excretion of sodium despite hyponatremia, (3) serum hypoosmolality, (4) urine osmolality that shows a significant degree of concentration (instead of the maximally dilute urine one would expect), (5) no evidence of blood volume depletion, and (6) normal renal and adrenal function (this criterion is necessary to rule out continuous sodium loss due to renal disease or Addison’s disease; diuretic-induced urine sodium loss should also be excluded). These criteria attempt to demonstrate that AVP (ADH) is secreted despite hemodilution, decreased serum osmolality, or both. The reason for increased sodium excretion is not definitely known; it is thought that increase of interstitial fluid volume by water retention may lead to suppression of sodium reabsorption (in order not to reabsorb even more water). Most patients with IADH syndrome do not have edema, since interstitial fluid expansion is usually only moderate in degree.

    In the diagnosis of IADH syndrome a problem may arise concerning what urine osmolality values qualify as a significant degree of concentration. If the serum and urine specimens are obtained at about the same time and the serum demonstrates significant hyponatremia and hypoosmolality, a urine osmolality greater than the serum osmolality is considered more concentrated than usual. However, in some cases of IADH syndrome the urine need not be higher than the serum osmolality for the diagnosis to be made, if it can be demonstrated that water retention is taking place despite a hypotonic plasma. With significant serum hypoosmolality, urine osmolality should be maximally dilute. This value is about 60-80 milliosmoles (mOsm)/L. A urine osmolality greater than 100 mOsm/L (literature range, 80-120 mOsm/L) can be considered a higher osmolality than expected under these circumstances. The urine sodium level is usually more than 20 mEq/L in patients with IADH syndrome, but can be decreased if the patient is on sodium restriction or has volume depletion. In patients with borderline normal or decreased urine sodium levels, the diagnosis of IADH may be assisted by administering a test dose of sodium. In IADH syndrome, infusion of 1,000 ml of normal saline will greatly increase urine sodium excretion but will not correct the hyponatremia as long as the patient does not restrict fluids (fluid restriction will cause sodium retention in IADH syndrome). Water restriction is the treatment of choice and may provide some confirmatory evidence. However, water restriction is not diagnostic, since it may also benefit patients with extracellular fluid (ECF) excess and edema. Uric acid renal clearance is increased in IADH syndrome, resulting in decreased serum uric acid levels in most, but not all, patients. Decreased serum uric acid levels in a patient with hyponatremia is another finding that is nondiagnostic but that raises the question of IADH syndrome.

    In some patients, assay of serum AVP (ADH) levels may be helpful to confirm the diagnosis. The AVP (ADH) levels should be elevated in IADH syndrome. However, AVP (ADH) assay is expensive, technically very difficult, and is available only in a few reference laboratories. The specimen should be placed immediately into a precooled anticoagulant tube, centrifuged at low temperature, frozen immediately, and sent to the laboratory packed in dry ice.

    IADH syndrome may be induced by a variety of conditions, such as: (1) central nervous system neoplasms, infections, and trauma; (2) various malignancies, most often in bronchogenic carcinoma of the undifferentiated small cell type (11% of patients); (3) various types of pulmonary infections; (4) several endocrinopathies, including myxedema and Addison’s disease; (5) certain medications, such as antineoplastics (vincristine, cyclophosphamide), oral antidiabetics (chlorpropamide, tolbutamide), hypnotics (opiates, barbiturates), and certain others such as carbamazepine; and (6) severe stress, such as pain, trauma, and surgery.

    Normal physiologic response to surgery is a temporary moderate degree of fluid and electrolyte retention, occurring at least in part from increased secretion of AVP (ADH). In the first 24 hours after surgery there tends to be decreased urine output, with fluid and electrolytes remaining in the body that would normally be excreted. Because of this, care should be taken not to overload the circulation with too much IV fluid on the first postoperative day. Thereafter, adequate replacement of normal or abnormal electrolyte daily losses is important, and excessive hypotonic fluids should be avoided. In certain patients, such as those undergoing extensive surgical procedures and those admitted originally for medical problems, it is often useful to obtain serum electrolyte values preoperatively so that subsequent electrolyte problems can be better evaluated.

  • Disorders of Arginine Vasopressin (Antidiuretic Hormone) Secretion

    Arginine Vasopressin (AVP, also called vasopressin; originally known as antidiuretic hormone or ADH) has been mentioned as one regulator of plasma volume by its ability to concentrate urine via its action on renal distal tubule water reabsorption. It is produced by the posterior pituitary under the influence of centers in the anterior hypothalamus. Several factors influence production: blood osmotic changes (concentration and dilution, acting on osmoreceptors in the hypothalamus), blood volume changes, certain neural influences such as pain, and certain drugs such as morphine and alcohol. The two most important syndromes associated with abnormal AVP (ADH) are diabetes insipidus and the “inappropriate ADH” syndrome.

    Diabetes Insipidus (DI) is a syndrome manifested by hypotonic polyuria. In spite of the name “diabetes,” it is not associated with diabetes mellitus, which produces a hypertonic polyuria (due to overexcretion of glucose). In general, there are three major etiologies of DI: neurogenic (hypothalamus unable to produce AVP [ADH] normally), renal (end-organ inability to respond normally to AVP [ADH], and temporary overpowering of the vasopressin system (ingestion of large quantities of water; sometimes called primary DI). Patients with DI are usually thirsty.

    Before starting a test sequence to determine etiology, it has been recommended that the following preliminary tests be done—24-hour urine collection for volume, osmolality, and solute excretion and serum sodium, potassium, calcium, and osmolality—all under basal conditions (unrestricted diet and water intake). The goals are to determine if polyuria exists (urine output over 2000 ml/day); if so, whether the urine is hypotonic (urine osmolality below 300 mosm/kg; literature range, 200-300 mosm/kg). If results show excess urine output that is hypotonic, the patient could have DI. Then the solute content per day should be measured. If the solute excretion is not increased (i.e., is less than 20 mosm/kg/day) the patient does not have a solute-induced diuresis and definitely qualifies for the diagnosis of DI. However, other relatively common etiologies for polyuria should be excluded, such as osmotic diuresis (glucose, NaC1, mannitol,) diuretics, hypokalemia, hypercalcemia, drug-induced (lithium, chlorpromazine, thioridazide), sickle cell disease, pregnancy-induced DI, severe chronic renal disease, or after acute tubular necrosis or renal transplantation. If the serum sodium or calcium level is high, this condition should be corrected before doing provocative tests. It is also necessary to stop any medications affecting AVP (ADH) secretion, all tobacco or alcohol use, and all caffeine-containing beverages at least 24 hours before and during the test. One investigator recommends blood osmolality measurement be done on plasma collected with heparin anticoagulant and tested using the freezing point depression method for best accuracy.

    The standard diagnostic procedure in DI is the water deprivation (dehydration) test. Although the basic procedure is followed throughout the literature, some details vary (such as the exact criteria for maximum dehydration, the minimum urine osmolality value acceptable as a response to maximal fluid-restriction dehydration, and the details of preparation for and starting the test. There are other test protocols in the literature to disclose etiology of DI; two of these will be presented, as well as the water deprivation test.

    1. Baseline serum osmolality and sodium levels that are high normal or elevated—serum osmolality over 295 mosm/kg (some investigators use 288 or 290) or sodium level over 143 mEq/L (mmol/L), with low urine osmolality (less than 300 mOsm/kg; literature range, 200-300)—are strong evidence against primary water-intake DI. The next step recommended is to inject subcutaneously either 1 µg of DDAVP (desmopressin, a synthetic analog of AVP) or 5 IU of AVP (vasopressin or ADH) and collect urine samples 30, 60, and 120 minutes afterward. If the highest urine osmolality after vasopressin is less than 50% higher than the baseline urine osmolality value, this suggests nephrogenic DI. If the result shows increase equal to or greater than 50%, this suggests neurogenic DI.

    2. It is also possible to differentiate between neurogenic, nephrogenic, and primary water intake etiologies for DI using administration of DDAVP for 2-3 days in a hospital with close observation. In patients with hypothalamic (neurogenic) DI there should be substantial decrease in thirst and urine output. In renal (nephrogenic) DI (primary polydipsia), there should be substantial decrease in urine output but increasing hyponatremia and body weight (due to continued high fluid intake). Although the simplicity of this test is attractive, it may be hazardous (especially in patients with primary polydipsia) and results are not always clear-cut.

    3. In the water deprivation test, the duration of water restriction is based on the degree of polyuria. The greater the output, the greater need for close supervision of the patient to prevent overdehydration. Patients with urine output less than 4000 ml/24 hours undergo restricted fluid after midnight; those with output greater than 4000 ml/24 hours begin fluid restriction at the time the test begins. Body weight and urine osmolality are measured hourly from 6 A.M. to noon or until three consecutive hourly determinations show urine osmolality increase of less than 30 mosm/kg (of H2O). The procedure should be terminated if body weight loss becomes more than 2 kg. When urine osmolality becomes stable, plasma osmolality is obtained. Osmolality should be greater than 288 mosm/kg for adequate dehydration. If this has occurred, 5 units of aqueous vasopressin (or 1 µg DDAVP) is administered subcutaneously. A urine specimen for osmolality is obtained 30-60 minutes after the injection. In central DI, there should be a rise in urine osmolality more than 9% of the last value before administration of vasopressin. In polyuria from nephrogenic DI, hypokalemia, or severe chronic renal disease, there is usually little increase in osmolality either during the dehydration test or after vasopressin administration. Patients with primary polydipsia frequently take longer than usual to dehydrate to a serum osmolality over 288, and urine osmolality rises less than 9% after vasopressin administration.

  • Dilutional Syndromes

    Cirrhosis is frequently associated with hyponatremia and hypokalemia, either separately or concurrently. There are a variety of etiologies: ascitic fluid sequestration; attempts at diuresis, often superimposed on poor diet or sodium restriction; paracentesis therapy; and hemodilution. Electrolyte abnormalities are more likely to appear when ascites is present and are more severe if azotemia complicates liver disease. Hemodilution is a frequent finding in cirrhosis, especially with ascites; this may be due to increased activity of aldosterone, which is normally deactivated in the liver, or sometimes is attributable to inappropriate secretion of AVP (ADH).

    Congestive heart failure is frequently associated with hyponatremia and much less frequently with hypokalemia. The most frequent cause of hyponatremia is overtreatment with diuretic therapy, usually in the context of dietary sodium restriction. However, sometimes the hyponatremia may be dilutional, due to retention of water as the glomerular filtration rate is decreased by heart failure or by inappropriate secretion of AVP (ADH). If hypokalemia is present, it usually is a side effect of diuretics.

  • Effects of Adrenal Cortex Dysfunction

    Certain adrenal cortex hormones control sodium retention and potassium excretion. Aldosterone is the most powerful of these hormones, but cortisone and hydrocortisone also have some effect. In primary Addison’s disease there are variable degrees of adrenal cortex destruction. This results in deficiency of both aldosterone and cortisol, thereby severely decreasing normal salt-retaining hormone influence on the kidney. Sometimes there is just enough hormone to maintain sodium balance at a low normal level. However, when placed under sufficient stress of any type, the remaining adrenal cortex cells cannot provide a normal hormone response and therefore cannot prevent a critical degree of sodium deficiency from developing. The crisis of Addison’s disease is the result of overwhelming fluid and salt loss from the kidneys and responds to adequate replacement. Serum sodium and chloride levels are low, the serum potassium level is usually high normal or elevated, and the patient is markedly dehydrated. The carbon dioxide (CO2) content may be normal or may be slightly decreased due to the mild acidosis that accompanies severe dehydration. In secondary Addison’s disease, due to pituitary insufficiency, glucocorticoid hormone production is decreased or absent but aldosterone production is maintained. However, hyponatremia sometimes develops due to an increase in AVP (ADH) production by the hypothalamus. In primary aldosteronism there is oversecretion of aldosterone, which leads to sodium retention and potassium loss. However, sodium retention is usually not sufficient to produce edema, and the serum sodium value remains within the reference range in more than 95% of cases. The serum potassium value is decreased in about 80% of cases (literature range, 34%-92%). In Cushing’s syndrome there is overproduction of hydrocortisone (cortisol), which leads to spontaneous mild hypokalemia and hypochloremic alkalosis in 10%-20% of patients (usually those with more severe degrees of cortisol excess). Use of diuretics will induce hypokalemia in other patients. The serum sodium level usually remains within reference range.

  • Hyponatremic Depletional Syndromes

    In protracted and severe vomiting, as occurs with pyloric obstruction or stenosis, gastric fluid is lost in large amounts and a hypochloremic (acid-losing) alkalosis develops. Gastric contents have a relatively low sodium content and water loss relatively exceeds electrolyte loss. Despite relatively low electrolyte content, significant quantities of electrolytes are lost with the fluid, leading to some depletion of total body sodium. The dehydration from fluid loss is partially counteracted by increased secretion of arginine vasopressin (AVP, or vasopressin; antidiuretic hormone, ADH) in response to decreased fluid volume. AVP promotes fluid retention. Whether hyponatremia, normal-range serum sodium values, or hypernatremia will develop depends on how much fluid and sodium are lost and the relative composition and quantity of replacement water and sodium, if any. Oral or parenteral therapy with sodium-free fluid tends to encourage hyponatremia. On the other hand, failure to supply fluid replacement may produce severe dehydration and even hypernatremia. Serum potassium values are most often low due to direct loss and to alkalosis that develops when so much hydrochloric acid is lost. Similar findings are produced by continuous gastric tube suction if continued over 24 hours.

    In severe or long-standing diarrhea, the most common acid-base abnormality is a base-losing acidosis. Fluid loss predominates quantitatively over loss of sodium, chloride, and potassium despite considerable depletion of total body stores of these electrolytes, especially of potassium. Similar to what occurs with vomiting, decrease in fluid volume by fluid loss is partially counteracted by increased secretion of AVP (ADH). Again, whether serum sodium becomes decreased, normal, or increased depends on degree of fluid and electrolyte loss and the amount and composition of replacement fluid (if any). Sufficient electrolyte-free fluids may cause hyponatremia. Little or no fluid replacement would tend toward dehydration, which, if severe, could even produce hypernatremia. The diarrhea seen in sprue differs somewhat from the electrolyte pattern of diarrhea from other causes in that hypokalemia is a somewhat more frequent finding.

    In extensive sweating, especially in a patient with fever, large amounts of water are lost. Although sweat consists mostly of water, there is a small but significant sodium chloride content. Enough sodium and chloride loss occurs to produce total body deficits, sometimes of surprising degree. The same comments previously made regarding gastrointestinal (GI) content loss apply here also.

    In extensive burns, plasma and extracellular fluid (ECF) leak into the damaged area in large quantities. If the affected area is extensive, hemoconcentration becomes noticeable and enough plasma may be withdrawn from the circulating blood volume to bring the patient close to or into shock. Plasma electrolytes accompany this fluid loss from the circulation. The fluid loss stimulates AVP (ADH) secretion. The serum sodium level may be normal or decreased, as discussed earlier. If the patient is supported over the initial reaction period, fluid will begin to return to the circulation after about 48 hours. Therefore, after this time, fluid and electrolyte replacement should be decreased, so as not to overload the circulation. Silver nitrate treatment for extensive burns may itself cause clinically significant hyponatremia (due to electrolyte diffusion into the hypotonic silver nitrate solution).

    Diabetic acidosis and its treatment provide very interesting electrolyte problems. Lack of insulin causes metabolism of protein and fat to provide energy that normally is available from carbohydrates. Ketone bodies and other metabolic acids accumulate; the blood glucose level is also elevated, and both glucose and ketones are excreted in the urine. Glucosuria produces an osmotic diuresis; a certain amount of serum sodium is lost with the glucose and water, and other sodium ions accompany the strongly acid ketone anions. The effects of osmotic diuresis, as well as of the accompanying electrolyte loss, are manifested by severe dehydration. Nevertheless, the serum sodium and chloride levels are often low in untreated diabetic acidosis, although (because of water loss) less often they may be within normal range. In contrast, the serum potassium level is usually normal. Even with normal serum levels, considerable total body deficits exist for all of these electrolytes. The treatment for severe diabetic acidosis is insulin and large amounts of IV fluids. Hyponatremia may develop if sufficient sodium and chloride are not given with the fluid to replace the electrolyte deficits. After insulin administration, potassium ions tend to move into body cells as they are no longer needed to combine with ketone acid anions. Also, potassium is apparently taken into liver cells when glycogen is formed from plasma glucose under the influence of insulin. In most patients, the serum potassium level falls to nearly one half the admission value after 3-4 hours of fluid and insulin therapy (if urine output is adequate) due to continued urinary potassium loss, shifts into body cells, and rehydration. After this time, potassium supplements should be added to the other treatment.

    Role of the kidney in electrolyte physiology

    In many common or well-recognized syndromes involving electrolytes, abnormality is closely tied to the role of the kidney in water and electrolyte physiology. A brief discussion of this subject may be helpful in understanding the clinical conditions discussed later.

    Urine formation begins with the glomerular filtrate, which is similar to plasma except that plasma proteins are too large to pass the glomerular capillary membrane. In the proximal convoluted tubules, about 85% of filtered sodium is actively reabsorbed by the tubule cells. The exchange mechanism is thought to be located at the tubule cell border along the side opposite the tubule lumen; thus, sodium is actively pumped out of the tubule cell into the renal interstitial fluid. Sodium from the urine passively diffuses into the tubule cell to replace that which is pumped out. Chloride and water passively accompany sodium from the urine into the cell and thence into the interstitial fluid. Most of the filtered potassium is also reabsorbed, probably by passive diffusion. At this time, some hydrogen ions are actively secreted by tubule cells into the urine but not to the extent that occurs farther down the nephron (electrolyte pathways and mechanisms are substantially less well known for the proximal tubules than for the distal tubules).

    In the ascending (thick) loop of Henle, sodium is still actively reabsorbed, except that the tubule cells are now impermeable to water. Therefore, since water cannot accompany reabsorbed sodium and remains behind in the urine, the urine at this point becomes relatively hypotonic (the excess of water over what would have been present had water reabsorption continued is sometimes called “free water” and from a purely theoretical point of view is sometimes spoken of as though it were a separate entity, almost free from sodium and other ions).

    In the distal convoluted tubules, three processes go on. First, sodium ions continue to be actively reabsorbed. (In addition to the sodium pump located at the interstitial side of the cell, which is pushing sodium out into the interstitial fluid, another transport mechanism on the tubule lumen border now begins actively to extract sodium from the urine into the tubule cells.) Intracellular hydrogen and potassium ions are actively excreted by the tubule cells into the urine in exchange for urinary sodium. There is competition between hydrogen and potassium for the same exchange pathway. However, since hydrogen ions are normally present in much greater quantities than potassium, most of the ions excreted into the urine are hydrogen. Second, the urinary acidification mechanisms other than bicarbonate reabsorption (NaHPO4 and NH4) operate here. Third, distal tubule cells are able to reabsorb water in a selective fashion. Permeability of the distal tubule cell to water is altered by a mechanism under the influence of AVP (ADH). There is a limit to the possible quantity of water reabsorbed, because reabsorption is passive; AVP (ADH) simply acts on cell membrane permeability, controlling the ease of diffusion. Therefore, only free water is actually reabsorbed.

    In the collecting tubules, the tubular membrane is likewise under the control of AVP (ADH). Therefore, any free water not reabsorbed in the distal convoluted tubules plus water that constitutes actual urine theoretically could be passively reabsorbed here. However, three factors control the actual quantity reabsorbed: (1) the state of hydration of the tubule cells and renal medulla in general, which determines the osmotic gradient toward which any reabsorbed water must travel; (2) the total water reabsorption capacity of the collecting tubules, which is limited to about 5% of the normal glomerular filtrate; and (3) the amount of free water reabsorbed in the distal convoluted tubules, which helps determine the total amount of water reaching the collecting tubules.

    Whether collecting tubule reabsorption capacity will be exceeded, and if so, to what degree, is naturally dependent on the total amount of water available. The amount of water reabsorbed compared to the degree of dilution (hypotonicity) of urine reaching the collecting tubules determines the degree of final urine concentration.

  • Hyponatremia. Iatrogenic Sources of Hyponatremia

    Diuretic therapy and administration of IV hypotonic fluids (dextrose in water or half-normal saline) form very important and frequent etiologies for hyponatremia, either as the sole agent or superimposed on some condition predisposing to hyponatremia. In several studies of patients with hyponatremia, diuretic use was considered to be the major contributing factor or sole etiology in about 30% of cases (range, 7.6%-46%). In two series of patients with severe hyponatremia (serum sodium <120 mEq/L), diuretics were implicated in 30%-73% of cases. Hyponatremia due to diuretics without any predisposing or contributing factors is limited mostly to patients over the age of 55 years. IV fluid administration is less often the sole cause for hyponatremia (although it occurs) but is a frequent contributing factor. In one study of postoperative hyponatremia, 94% of the patients were receiving hypotonic fluids. If renal water excretion is impaired, normal maintenance fluid quantities may lead to dilution, whereas excessive infusions may produce actual water intoxication or pulmonary edema. There may also be problems when excessive losses of fluid or various electrolytes occur for any reason and replacement therapy is attempted but either is not adequate or is excessive. The net result of any of the situations mentioned is a fluid disorder with or without an electrolyte problem that must be carefully and logically reasoned out, beginning from the primary deficit (the cause of which may still be active) and proceeding through subsequent events. Adequate records of fluid and electrolyte administration are valuable in solving the problem. In nonhospitalized persons a similar picture may be produced by dehydration with conscious or unconscious attempts at therapy by the patient or relatives. For example, marked sweating leads to thirst, but ingestion of large quantities of water alone dilutes body fluid sodium, already depleted, even further. A baby with diarrhea may be treated at home with water or sugar water; this replaces water but does not adequately replace electrolytes and so has the same dilutional effect as in the preceding example. On the other hand, the infant may be given boiled skimmed milk or soup, which are high-sodium preparations; the result may be hypernatremia if fluid intake is not adequate.

  • Serum Sodium Abnormalities

    The most frequent electrolyte abnormalities, both clinically and as reflected in abnormal laboratory values, involve sodium. This is true because sodium is the most important cation of the body, both from a quantitative standpoint and because of its influence in maintaining electric neutrality. The most common causes of low or high serum sodium values are enumerated in the box. Some of these conditions and the mechanisms involved require further explanation.

    Technical problems in sodium measurement may affect results. For many years the primary assay technique for sodium and potassium was flame photometry. Since 1980, instrumentation has been changing to ion-selective electrodes (ISEs). ISEs generate sodium results that are about 2% higher than those obtained by flame photometry (in patient blood specimens this difference is equivalent to 2-3 mEq/L [2-3 mmol/L]). Potassium values are about the same with both techniques. Many, but not all, laboratories automatically adjust their ISE sodium results to make them correspond to flame photometer values. Sodium concentration can be decreased in blood by large amounts of glucose (which attracts intracellular fluid, creating a dilutional effect). Each 62 mg of glucose/100 ml (3.4 mmol/L) above the serum glucose upper reference limit results in a decrease in serum sodium concentration of 1.0 mEq/L. Large amounts of serum protein (usually in patients with myeloma) or lipids (triglyceride concentration >1,500 mg/100 ml [17 mmol/L]) can artifactually decrease the serum sodium level when sodium is measured by flame photometry (values obtained by the ISE method are not affected). One report suggests a formula whose result can be added to flame photometry values to correct for severe

    Clinical Situations Frequently Associated With Serum Sodium Abnormalities

    I. Hyponatremia
    A. Sodium and water depletion (deficit hyponatremia)
    1. Loss of gastrointestinal (GI) secretions with replacement of fluid but not electrolytes
    a. Vomiting
    b. Diarrhea
    c. Tube drainage
    2. Loss from skin with replacement of fluids but not electrolytes
    a. Excessive sweating
    b. Extensive burns
    3. Loss from kidney
    a. Diuretics
    b. Chronic renal insufficiency (uremia) with acidosis
    4. Metabolic loss
    a. Starvation with acidosis
    b. Diabetic acidosis
    5. Endocrine loss
    a. Addison’s disease
    b. Sudden withdrawal of long-term steroid therapy
    6. Iatrogenic loss from serous cavities
    a. Paracentesis or thoracentesis
    B. Excessive water (dilution hyponatremia)
    1. Excessive water administration
    2. Congestive heart failure
    3. Cirrhosis
    4. Nephrotic syndrome
    5. Hypoalbuminemia (severe)
    6. Acute renal failure with oliguria
    C. Inappropriate antidiuretic hormone (IADH) syndrome
    D. Intracellular loss (reset osmostat syndrome)
    E. False hyponatremia (actually a dilutional effect)
    1. Marked hypertriglyceridemia*
    2. Marked hyperproteinemia*
    3. Severe hyperglycemia
    II. Hypernatremia
    Dehydration is the most frequent overall clinical finding in hypernatremia.
    1. Deficient water intake (either orally or intravenously)
    2. Excess kidney water output (diabetes insipidus, osmotic diuresis)
    3. Excess skin water output (excess sweating, loss from burns)
    4. Excess gastrointestinal tract output (severe protracted vomiting or diarrhea without fluid therapy)
    5. Accidental sodium overdose
    6. High-protein tube feedings

    *Artifact in flame photometry, not in ISE.

    hyperlipidemia (triglyceride >1,500 mg/100 ml): % that Na value should increase = 2.1 Ч [triglyceride (gm/100 ml) – 0.6]. There is an interesting and somewhat inexplicable variance in reference range values for sodium in the literature, especially for the upper end of the range. This makes it highly desirable for each laboratory to determine its own reference range. Another problem is a specimen drawn from the same arm that already has an intravenous (IV) line; this usually happens when the phlebotomist cannot find a vein in the opposite arm. However, this may lead to interference by the contents of the IV system.